The research in progress is designed to ascertain the pathogenesis of early (first 48 hours) fluid volume changes following major thermal injury (burns greater than 20% TBSA) and the subsequent course of fluid volume and electrolyte mobilization and excretion. Specifically, the inter-relationships of significant hemodynamic, hematologic, and metabolic abnormalities affecting both phases of fluid changes in both experimental and clinical burns. Serial measurements of extracellular fluid volume (S35) and blood volume (I125, CR51), cardiac output, and organ flow determinations (micro-bead) as well as intracellular fluid and electrolyte changes (transmembrane potential and serial muscle cell electrolytes) are being determined in experimental burns (40% flame burn in baboons) and in clinical patients. Simultaneously the role of fibrinogen degradation products from extravascular clotting are isolated and separated by sephadex column and gel-electrophoresis and studied in relationship to the myocardial depression (Langendorf profusion) production of burn wound edema (polymerization) and organ blood flow changes. Finally, the hypermetabolism of burns as it relates to these changes is being correlated by studies of decreased oxygen consumption of leukocytes, enzyme activation and ATP utilization.